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This study aimed to identify inflammatory cytokines involved in driving Tfh cell responses in systemic lupus erythematosus (SLE).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      The circulating Tfh frequencies and interferon (IFN)\u2010\u03b2 levels were analyzed for correlations with disease activities in patients with SLE. Both lupus mice with IFN\u2010\u03b2 treatment and Ifnar1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice with lupus induction were assessed for Tfh cell responses and disease progression. Sorting\u2010purified naive CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells from Ifnar1\n                      <jats:sup>\u2212\/\u2212<\/jats:sup>\n                      mice were adoptively transferred to lupus mice for monitoring Tfh cell differentiation in vivo. In culture, mouse CD4\n                      <jats:sup>+<\/jats:sup>\n                      T cells treated with IFN\u2010\u03b2 were examined for Tfh cell differentiation and intracellular signaling pathway. The underlying mechanism for IFN\u2010\u03b2 secretion by myeloid\u2010derived suppressor cells (MDSCs) was investigated by co\u2010immunoprecipitation and Western blotting.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>We found that increased Tfh cells with IFN\u2010I\u2013inducible gene signatures correlated with disease activities in patients with SLE. Consistently, IFN\u2010\u03b2 treatment markedly enhanced Tfh cell response and exacerbated disease progression in lupus mice. Moreover, mice with IFNAR1 deficiency exhibited attenuated lupus progression with significantly decreased Tfh response. Mechanistically, IFN\u2010\u03b2 activated the indoleamine 2,3\u2010dioxygenase\/kynurenine\/aryl hydrocarbon receptor (IDO\/Kyn\/AhR)\u00a0axis to promote Tfh cell differentiation. Notably, expanded MDSCs in lupus were found to produce high levels of IFN\u2010\u03b2. Further studies showed that the autoantigen activated lymphocyte\u2010derived DNA stimulated IFN\u2010\u03b2 production by MDSCs via the cyclic GMP\u2010AMP synthase\u2013stimulator of IFN genes (cGAS\u2010STING)\u2013dependent pathway.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>These results have demonstrated a novel function of IFN\u2010\u03b2 in promoting Tfh cell response during lupus progression, which may facilitate the identification of new therapeutic targets for the treatment of SLE.<\/jats:p>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/art70004-gra-0001-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/art.70004","type":"journal-article","created":{"date-parts":[[2025,11,28]],"date-time":"2025-11-28T09:54:53Z","timestamp":1764323693000},"page":"1088-1101","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Myeloid\u2010Derived Suppressor Cell\u2013Derived Interferon\u2010\u03b2 Promotes T Follicular Helper Cell Response and Exacerbates Lupus Development"],"prefix":"10.1002","volume":"78","author":[{"given":"Ke","family":"Rui","sequence":"first","affiliation":[{"name":"Department of Laboratory Medicine Affiliated Hospital of Jiangsu University  Zhenjiang China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zixiang","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of 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